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			PubMed Journals: J Virol

  Source:		PMID: 15681410
  Download:	https://www.ncbi.nlm.nih.gov/pmc/articles/PMC546554/pdf/1306-04.pdf

    		J Virol. 2005 Feb;79(4):2079-86.
     
			Inhibition of Beta interferon induction by
			severe acute respiratory syndrome coronavirus
			suggests a two-step model for activation
			of interferon regulatory factor 3.

			Spiegel M(1), Pichlmair A, Martínez-Sobrido
			L, Cros J, García-Sastre A, Haller O, Weber
			F.

			Author Information
			(1) Abteilung Virologie, Institut für Medizinische
			Mikrobiologie und Hygiene, Universität Freiburg,
			D-79008 Freiburg, Germany.

			Severe acute respiratory syndrome (SARS) is
			caused by a novel coronavirus termed SARS-CoV.
			We and others have previously shown that
			the replication of SARS-CoV can be suppressed
			by exogenously added interferon (IFN), a
			cytokine which is normally synthesized by
			cells as a reaction to virus infection.
			Here, we demonstrate that SARS-CoV escapes
			IFN-mediated growth inhibition by preventing
			the induction of IFN-beta. In SARS-CoV-infected
			cells, no endogenous IFN-beta transcripts
			and no IFN-beta promoter activity were detected.
			Nevertheless, the transcription factor
			interferon regulatory factor 3 (IRF-3),
			which is essential for IFN-beta promoter
			activity, was transported from the cytoplasm
			to the nucleus early after infection with
			SARS-CoV. However, at a later time point
			in infection, IRF-3 was again localized
			in the cytoplasm. By contrast, IRF-3 remained
			in the nucleus of cells infected with the
			IFN-inducing control virus Bunyamwera delNSs.
			Other signs of IRF-3 activation such as
			hyperphosphorylation, homodimer formation,
			and recruitment of the coactivator
			CREB-binding protein (CBP) were found late
			after infection with the control virus but
			not with SARS-CoV. Our data suggest that
			nuclear transport of IRF-3 is an immediate-early
			reaction to virus infection and may precede
			its hyperphosphorylation, homodimer formation,
			and binding to CBP. In order to escape activation
			of the IFN system, SARS-CoV appears to block
			a step after the early nuclear transport
			of IRF-3.

			DOI: 10.1128/JVI.79.4.2079-2086.2005
			PMCID: PMC546554 PMID: 15681410 [Indexed
			for MEDLINE]

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